Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse

Detalhes bibliográficos
Autor(a) principal: Preite, Nailliw Zanini [UNIFESP]
Data de Publicação: 2016
Outros Autores: Nascimento, Bruna Pascarelli Pedrico do [UNIFESP], Muller, Cynthia R., Americo, Anna Laura V., Higa, Talita S., Evangelista, Fabiana S., Lancellotti, Carmen L., Henriques, Felipe dos Santos, Batista, Miguel Luiz, Jr., Bianco, Antonio C., Ribeiro, Miriam O.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
dARK ID: ark:/48912/001300000z13b
Texto Completo: http://dx.doi.org/10.1530/JOE-16-0199
https://repositorio.unifesp.br/handle/11600/56682
Resumo: The brown adipose tissue (BAT) mediates adaptive changes in metabolic rate by responding to the sympathetic nervous system through beta-adrenergic receptors (AR). Here, we wished to define the role played by the AR beta(3) isoform in this process. This study focused on the AR beta(3) knockout mice (AR beta 3KO), including responsiveness to cold exposure, diet-induced obesity, intolerance to glucose, dyslipidaemia and lipolysis in white adipose tissue (WAT). AR beta 3KO mice defend core temperature during cold exposure (4 degrees C for 5h), with faster BAT thermal response to norepinephrine (NE) infusion when compared with wild-type (WT) mice. Despite normal BAT thermogenesis, AR beta 3KO mice kept on a high-fat diet (HFD
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spelling Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouseobesitylipolysisadaptive thermogenesisbrown adipose tissuebeta(3) adrenergic receptorThe brown adipose tissue (BAT) mediates adaptive changes in metabolic rate by responding to the sympathetic nervous system through beta-adrenergic receptors (AR). Here, we wished to define the role played by the AR beta(3) isoform in this process. This study focused on the AR beta(3) knockout mice (AR beta 3KO), including responsiveness to cold exposure, diet-induced obesity, intolerance to glucose, dyslipidaemia and lipolysis in white adipose tissue (WAT). AR beta 3KO mice defend core temperature during cold exposure (4 degrees C for 5h), with faster BAT thermal response to norepinephrine (NE) infusion when compared with wild-type (WT) mice. Despite normal BAT thermogenesis, AR beta 3KO mice kept on a high-fat diet (HFD40% fat) for 8 weeks exhibited greater susceptibility to diet-induced obesity, markedly increased epididymal adipocyte area with clear signs of inflammation. The HFD-induced glucose intolerance was similar in both groups but serum hypertriglyceridemia and hypercholesterolemia were less intense in AR beta 3KO animals when compared with WT controls. Isoproterenol-induced lipolysis in isolated white adipocytes as assessed by glycerol release was significantly impaired in AR beta 3KO animals despite normal expression of key proteins involved in lipid metabolism. In conclusion, AR beta(3) inactivation does not affect BAT thermogenesis but increases susceptibility to diet-induced obesity by dampening WAT lipolytic response to adrenergic stimulation.Univ Prebiteriana Mackenzie, Ctr Biol & Hlth Sci, Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Dept Translat Med, EPM, Sao Paulo, SP, BrazilUniv Sao Paulo, Expt Pathophysiol Dept, Fac Med, BR-05508 Sao Paulo, SP, BrazilUniv Sao Paulo, Sch Arts Sci & Humanities, Sao Paulo, SP, BrazilSch Med Sci, Dept Pathol, Sao Paulo, SP, BrazilUniv Mogi das Cruzes, Integrated Grp Biotechnol, Lab Adipose Tissue Biol, Mogi Das Cruzes, SP, BrazilRush Univ & Med Ctr, Dept Internal Med, Div Endocrinol & Metab, Chicago, IL USADepartment of Translational Medicine, EPM, Universidade Federal de São Paulo (UNIFESP), Sao Paulo, SP, BrazilWeb of ScienceFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)FAPESP: 2009/50353-1FAPESP: 2015/19259-0Bioscientifica Ltd2020-07-31T12:47:14Z2020-07-31T12:47:14Z2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion259-269http://dx.doi.org/10.1530/JOE-16-0199Journal Of Endocrinology. Bristol, v. 231, n. 3, p. 259-269, 2016.10.1530/JOE-16-01990022-0795https://repositorio.unifesp.br/handle/11600/56682WOS:000387982200009ark:/48912/001300000z13bengJournal Of EndocrinologyBristolinfo:eu-repo/semantics/openAccessPreite, Nailliw Zanini [UNIFESP]Nascimento, Bruna Pascarelli Pedrico do [UNIFESP]Muller, Cynthia R.Americo, Anna Laura V.Higa, Talita S.Evangelista, Fabiana S.Lancellotti, Carmen L.Henriques, Felipe dos SantosBatista, Miguel Luiz, Jr.Bianco, Antonio C.Ribeiro, Miriam O.reponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2022-02-10T21:18:19Zoai:repositorio.unifesp.br/:11600/56682Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-12-11T20:44:27.413595Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
title Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
spellingShingle Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
Preite, Nailliw Zanini [UNIFESP]
obesity
lipolysis
adaptive thermogenesis
brown adipose tissue
beta(3) adrenergic receptor
title_short Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
title_full Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
title_fullStr Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
title_full_unstemmed Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
title_sort Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
author Preite, Nailliw Zanini [UNIFESP]
author_facet Preite, Nailliw Zanini [UNIFESP]
Nascimento, Bruna Pascarelli Pedrico do [UNIFESP]
Muller, Cynthia R.
Americo, Anna Laura V.
Higa, Talita S.
Evangelista, Fabiana S.
Lancellotti, Carmen L.
Henriques, Felipe dos Santos
Batista, Miguel Luiz, Jr.
Bianco, Antonio C.
Ribeiro, Miriam O.
author_role author
author2 Nascimento, Bruna Pascarelli Pedrico do [UNIFESP]
Muller, Cynthia R.
Americo, Anna Laura V.
Higa, Talita S.
Evangelista, Fabiana S.
Lancellotti, Carmen L.
Henriques, Felipe dos Santos
Batista, Miguel Luiz, Jr.
Bianco, Antonio C.
Ribeiro, Miriam O.
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Preite, Nailliw Zanini [UNIFESP]
Nascimento, Bruna Pascarelli Pedrico do [UNIFESP]
Muller, Cynthia R.
Americo, Anna Laura V.
Higa, Talita S.
Evangelista, Fabiana S.
Lancellotti, Carmen L.
Henriques, Felipe dos Santos
Batista, Miguel Luiz, Jr.
Bianco, Antonio C.
Ribeiro, Miriam O.
dc.subject.por.fl_str_mv obesity
lipolysis
adaptive thermogenesis
brown adipose tissue
beta(3) adrenergic receptor
topic obesity
lipolysis
adaptive thermogenesis
brown adipose tissue
beta(3) adrenergic receptor
description The brown adipose tissue (BAT) mediates adaptive changes in metabolic rate by responding to the sympathetic nervous system through beta-adrenergic receptors (AR). Here, we wished to define the role played by the AR beta(3) isoform in this process. This study focused on the AR beta(3) knockout mice (AR beta 3KO), including responsiveness to cold exposure, diet-induced obesity, intolerance to glucose, dyslipidaemia and lipolysis in white adipose tissue (WAT). AR beta 3KO mice defend core temperature during cold exposure (4 degrees C for 5h), with faster BAT thermal response to norepinephrine (NE) infusion when compared with wild-type (WT) mice. Despite normal BAT thermogenesis, AR beta 3KO mice kept on a high-fat diet (HFD
publishDate 2016
dc.date.none.fl_str_mv 2016
2020-07-31T12:47:14Z
2020-07-31T12:47:14Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1530/JOE-16-0199
Journal Of Endocrinology. Bristol, v. 231, n. 3, p. 259-269, 2016.
10.1530/JOE-16-0199
0022-0795
https://repositorio.unifesp.br/handle/11600/56682
WOS:000387982200009
dc.identifier.dark.fl_str_mv ark:/48912/001300000z13b
url http://dx.doi.org/10.1530/JOE-16-0199
https://repositorio.unifesp.br/handle/11600/56682
identifier_str_mv Journal Of Endocrinology. Bristol, v. 231, n. 3, p. 259-269, 2016.
10.1530/JOE-16-0199
0022-0795
WOS:000387982200009
ark:/48912/001300000z13b
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Journal Of Endocrinology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 259-269
dc.coverage.none.fl_str_mv Bristol
dc.publisher.none.fl_str_mv Bioscientifica Ltd
publisher.none.fl_str_mv Bioscientifica Ltd
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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